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Vitamins, Fat-Soluble
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Because they dissolve in fat, vitamins A, D, E, and K are called fat-soluble vitamins. They are absorbed
from the small intestines, along with dietary fat, which is why fat malabsorption resulting from various
diseases (e.g., cystic fibrosis, ulcerative colitis, Crohn's disease) is associated with poor absorption of
these vitamins. Fat-soluble vitamins are primarily stored in the liver and adipose tissues. With the
exception of vitamin K, fat-soluble vitamins are generally excreted more slowly than water-soluble
vitamins, and vitamins A and D can accumulate and cause toxic effects in the body.
Vitamin A
Vitamin A was the first fat-soluble vitamin identified (in 1913). Vitamin A comprises the preformed
retinoids, plus the precursor forms, the provitamin A carotenoids. Preformed retinoids is a collective term
for retinol, retinal, and retinoic acid, all of which are biologically active. The provitamin A carotenoids
include beta-carotene and others, which are converted to retinoids with varying degrees of efficiency.
Retinoids are sensitive to heat, light, and oxidation by air. Beta-carotene is relatively more stable. Vitamin
E helps protect vitamin A from oxidation. There is some loss of vitamin A with cooking, but only after
boiling for a comparatively long period.
Retinoids are converted to retinol in the intestines and transported with dietary fat to the liver, where it
is stored. A special transport protein, retinolbinding protein (RBP), transports vitamin A from the liver to
other tissues. Carotenoids are absorbed intact at a much lower absorption rate than retinol. Of all the
carotenoids, beta-carotene has the highest potential vitamin-A activity. The active forms of vitamin A
have three basic functions: vision, growth and development of tissues, and immunity.



Vision. Vitamin A combines with a protein called opsin to form rhodopsin in the rod cells of the
retina. When vitamin A is inadequate, the lack of rhodopsin makes it difficult to see in dim light.
Growth and development of tissues. Vitamin A is involved in normal cell differentiation—a process
through which embryonic cells transform into mature tissue cells with highly specific functions.
Vitamin A supports male and female reproductive processes and bone growth.
Immunity. Vitamin A is essential for immune function and vitamin-A deficiency is associated
with decreased resistance to infections. The severity of some infections, such as measles and
diarrhea, is reduced by vitamin-A supplementation among those who suffer from vitamin-A
deficiency.
FAT SOLUBLE VITAMINS
Vitamin
Functions
Deficiency
symptoms
People at risk Sources
Daily
recommended
intakes
Toxicity
SOURCE Wardlaw, Gordon M.; Hampl, Jeffrey S.; and Disilvestro, Robert A. (2004). Perspectives in Nutrition, 6th
edition. New York: McGraw-Hill.
Vitamin
A
Preformed
retinoids and
provitamin A
carotinoids
Vision in dim
light and color
vision,
cell
differentiation
and growth,
immunity
Poor growth,
night
blindness,
blindness, dry
skin,
Xerophthalmia
Rare
in
United States
but common
in preschool
children
living
in
poverty
in
Preformed
vitamin
A:
liver, fortified
milk, fish liver
oils Provitamin
A: red, orange,
dark green, and
Infants:
400-500
mg RAE Children:
300-400 mg RAE
Adolescents: 600900 mg RAE Adult
men & women:
700-900 mg RAE
Headache,
vomiting,
double
vision, hair
loss,
dry
mucous
membranes,
Vitamin
Functions
Deficiency
symptoms
People at risk Sources
Daily
recommended
intakes
Toxicity
developing
countries,
alcoholics
Pregnant women:
750-770 mg RAE
Lactating
women:1200-1300
mg RAE
bone
and
joint pain,
fractures,
liver
damage,
hemorrhage,
coma,
teratogenic
effects:
spontaneous
abortions,
birth
defects.
Upper level
is 3000 mg
of
preformed
vitamin A
based
on
risk of birth
defects and
liver
toxicity.
yellow
vegetables,
orange fruits
Vitamin
D Maintainence Rickets
in
Cholecalciferol of
children,
Ergocalciferol intracellular
osteomalacia
and
in older adults
extracellular
calcium
concentrations
Dark skinned Vitamin
individuals,
fortified
older adults, fish oils
breastfed
infants from
vitamin
D
deficient
mother
Vitamin
E Antioxidant,
Tocopherols
prevention of
Tocotrienols
propagation
of
free
radicals
Patients with
fat
malabsorption
syndromes,
smokers
[overt
deficiency is
rare]
Plant
oils, Infants: 4-5 mg
seeds,
nuts, Children: 6-7 mg
products made Adolescents:11-15
from oils
mg Adult men &
women: 15 mg
Pregnant women:
15 mg Lactating
women: 19 mg
Those taking
antibiotics for
a long period
of time; older
adults
with
scant
green
vegetable
intake
Green
vegetables,
liver synthesis
by
intestinal
microorganisms
Hemolysis of
red
blood
cells,
degeneration
of
sensory
neurons
Vitamin
K Synthesis of Hemorrhage,
Phylloquinone blood clotting fractures
Menaquinone factors
and
bone proteins
D 0-50 years: 5 mg Calcification
milk, 51-70 years: 10 mg, of
soft
>70 years: 15 mg
tissues,
growth
restriction,
excess
calcium
excretion
via
the
kidney.
Upper level
is 50 mg
based on the
risk elevated
blood
calcium.
Inhibition of
vitamin K
metabolism.
Upper level
is 1000 mg
based on the
risk
of
hemorrhage.
Infants: 2-2.5 mg No
upper
Children:
30-55 level
has
mg Adolescents: been set
60-75 mg Adult
men: 90 mg Adult
women: 120 mg
Pregnant/lactating
women: 75-90 mg
It has been suggested that beta-carotene and other carotenoids (also called phytochemicals) may
function as antioxidants by neutralizing free radicals. Free radicals are unstable, highly reactive
molecules that damage DNA, cause cell injury, and increase the risk of chronic disease. Beta-carotene
has also been associated with reducing the risk of lung cancer. Lutein and zeaxanthin, yellow carotenoid
pigments in corn and dark green leafy vegetables, may reduce the risk of macular degeneration and
agerelated cataracts. Lycopene, a red carotenoid pigment in tomatoes, may help reduce the risk of
prostrate cancer, cardiovascular disease, and skin damage from sunlight.
Deficiency.
Dietary deficiency of vitamin A is rare in North America and western Europe, but it is the leading cause
of blindness in children worldwide. Newborn and premature infants, the urban poor, older adults,
people with alcoholism or liver disease, and those with fat malabsorption syndrome are all at increased
risk.
One of the earliest symptoms of vitamin-A deficiency is night blindness. It is a temporary condition, but
if left untreated it can cause permanent blindness. This degeneration is called xerophthalmia, and it
usually occurs in children after they are weaned. Symptoms include dryness of the cornea and eye
membranes due to lack of mucus production, which leaves the eye vulnerable to surface dirt and
bacterial infections. Vitamin-A deficiency can cause follicular hyperkeratosis, a condition in which hair
follicles become plugged with keratin, giving a bumpy appearance and a rough, dry texture to skin.
In developing countries, the severity of infectious diseases such as measles is often correlated to the
degree of vitamin-A deficiency. Providing large doses of vitamin A reduces the risk of dying from these
infections. The age range of the target population for vitamin-A intervention programs is usually from
birth to seven years. Administration of high-potency doses in the range of 15,000 to 60,000 micrograms
(μg) are distributed to young children in targeted areas of the world to build up liver stores for up to six
months. However, consumption of adequate food sources is the most important long-term solution to
vitamin-A deficiency.
Toxicity.
Vitamin-A toxicity, called hypervitaminosis A, can result from long-term supplementation of two to four
times the RDA for preformed vitamin A. Excess intake of preformed vitamin A is a teratogen, meaning it
can cause birth defects. Birth defects associated with vitamin-A toxicity include cleft palate, heart
abnormalities, and brain malfunction. Acute excess intake during pregnancy can also cause spontaneous
abortions. Pregnant women should avoid prenatal supplements containing retinal, as well as
medications made from retinoids, such as Accutane and Retin-A. Prolonged and excessive consumption
of carotene-rich foods can lead to hypercarotenemia, a clinical condition characterized by deep orange
discoloration of the skin and increased carotene levels in the blood. This condition is usually harmless.
Vitamin D (Calciferol)
In the seventeenth century, vitamin-D deficiency was so common in British children that it came to be
known as "children's disease of the English." In
Sunlight stimulates the synthesis of vitamin D, which regulates the body's absorption of calcium and
therefore is essential to skeletal health. Just fifteen minutes in the sun several times weekly is sufficient.
After that, sunscreen should be applied to avoid ultraviolet damage to the skin.
[Photograph by Michael Keller. Corbis. Reproduced by permission.]
the mid-1800s, cod liver oil became well known for treating this disease. In 1925, Elmer McCollum and
coworkers determined that the "antirachitic" (antirickets) substance in cod liver oil was vitamin D.
Because vitamin D is relatively stable in foods, many countries fortify milk with vitamin D to help
prevent rickets. However, significant losses may result from fortified milk exposed to light.
Vitamin D from foods is absorbed from the upper part of the small intestine, along with dietary fat, and
transported to the liver. In the skin, ultraviolet (UV) radiation from the sun converts a cholesterol
derivative to cholecalciferol, which enters the blood stream and is transported to the liver. In the liver,
vitamin D is converted to calcidiol, an inactive form that circulates in blood. Kidneys take up calcidiol
and convert it to an active hormone form of vitamin D called calcitriol. People with chronic kidney
failure have very low levels of calcitriol and must be routinely treated with this form of the vitamin.
The best-known function of active vitamin D is to help regulate blood levels of calcium and
phosphorous. Vitamin D increases absorption of these minerals from the gastrointestinal (GI) tract. In
combination with parathyroid hormone, it enhances their reabsorption from the kidneys and their
mobilization from bones into the blood. Vitamin D helps maintain calcium levels even if dietary intakes
are not optimal. Calcitriol affects growth of normal cells and some cancer cells. Adequate vitamin-D
status has been linked to a reduced risk of developing breast, colon, and prostrate cancers.
Deficiency.
Long-term deficiency of vitamin D affects the skeletal system. In children, vitamin-D deficiency leads to
rickets, a condition in which bones weaken and bow under pressure. Although vitamin-D fortification
has reduced incidence of rickets in North America, it is sometimes seen in children with malabsorption
syndrome and is still common in many parts of the world. In adults, vitamin-D deficiency causes
osteomalacia, or "soft bones," increasing the risk for fractures in hip, spine, and other bones. Vitamin-D
deficiency also contributes to osteoporosis. In elderly persons, vitamin-D supplementation reduces the
risk of osteoporotic fractures.
Infants are born with stores of vitamin D that last about six months. Breast milk contains very little
vitamin D, however, and infants beyond six months of age who are exclusively breastfed must obtain
vitamin D via exposure to sunlight or a supplement given under the guidance of a physician.
Older adults are especially at risk for vitamin-D deficiency for several reasons. The skin, liver, and
kidneys lose their capacity to synthesize and activate vitamin D with advancing age, and older adults
typically drink little or no milk, a major dietary source of vitamin D. Older adults also rarely venture
outdoors, and when they do, they apply sunscreen to exposed areas of the body, further contributing to
the decline in vitamin-D synthesis in the skin.
Sunscreens with a sun protection factor (SPF) of 8 and above prevent vitamin-D synthesis. Sunscreen
should be applied only after enough time has elapsed to provide sufficient vitamin-D synthesis.
Exposure to the sun does not cause vitamin-D toxicity, and for most people, exposing the hands, face,
and arms on a clear summer day for fifteen minutes a few times a week should provide sufficient
Vitamin D. Dark-skinned people require longer sunlight exposure because melanin, a skin pigment, is a
natural sunscreen.
Dietary recommendations assume that no vitamin D is available from exposure to sunlight. Thus, people
who do not venture outdoors or who live in northern or predominantly cloudy climates need to pay
attention to dietary sources. Plants are poor sources of vitamin D, so strict vegetarians must meet their
vitamin-D needs through exposure to sunlight, fortification, or supplementation.
Toxicity.
Vitamin D is most likely to have toxic effects when consumed in excessive amounts through
supplementation. Excess vitamin D raises blood calcium levels, resulting in calcium precipitation in soft
tissues and stone formation in the kidneys, where calcium becomes concentrated in an effort to excrete it.
Vitamin K
In 1929, the Danish researcher Henrik Dam first noted that vitamin K played a critical role in blood
clotting, and he named it vitamin "K" for "Koagulation." Vitamin K comprises a family of compounds
known as quinones. These include phylloquinone from plants and the menaquinones from animal sources.
Phylloquinone is the most biologically active form. Menaquinones are also synthesized by bacteria in the
colon and absorbed, contributing about 10 percent of total vitamin-K needs. Vitamin-K absorption
depends on normal consumption and digestion of dietary fat. It is primarily stored in the liver.
Vitamin K helps in the activation of seven blood-clotting-factor proteins that participate in a series of
reactions to form a clot that eventually stops the flow of blood. Vitamin K also participates in the
activation of bone proteins, which greatly enhances their calcium-binding properties. Low levels of
circulating vitamin K have been associated with low bone-mineral density. Thus, an adequate intake of
vitamin K may help protect against hip fractures.
Deficiency.
A primary deficiency of vitamin K is rare, but a secondary deficiency may result from fat malabsorption
syndrome. Prolonged use of antibiotics can destroy the intestinal bacteria that produce vitamin K,
precipitating deficiency in individuals at risk. Newborn infants are born with a sterile intestinal tract and
those who are breastfed, may run the risk of vitamin-K deficiency, since breast-milk production takes a
few days to establish and breast milk is naturally low in this vitamin. To prevent hemorrhaging, all
infants in North America receive injections of vitamin K within six hours of birth.
Toxicity.
High doses of vitamin K can reduce the effectiveness of anticoagulant drugs such as warfarin
(Coumadin), which is used to prevent blood clotting. People taking these drugs should maintain a
consistent daily intake of vitamin K. Megadose supplements of vitamin A and E can pose a risk to
vitamin-K status. Vitamin A interferes with absorption of vitamin K, and large doses of vitamin E
decrease vitamin K–dependent clotting factors, thus promoting bleeding. Toxicity from food is rare,
because the body excretes vitamin K much more rapidly than other fat-soluble vitamins.
Vitamin E
The link between vitamin-E deficiency and reproductive failure in rats was first discovered in 1922 by
Herbert Evans and Katherine Scott Bishop. The chemical name of vitamin E, tocopherol, is derived from
toco, meaning "related to childbirth."
Vitamin E comprises a family of eight naturally occurring compounds: four tocopherols and four
tocotrienols, of which alpha-tocopherol is the only one to have vitamin-E activity in the human body. It is
also the most common form of vitamin E in food. Vitamin E is highly susceptible to destruction by
oxygen, metals, light, and deep-fat frying. As a result, prolonged food storage lowers the vitamin-E
content of food.
As with other fat-soluble vitamins, absorption of vitamin E requires adequate absorption of dietary fat.
In addition, the percentage of absorption declines as the amount consumed is increased. Vitamin E is
stored mainly in adipose tissue, while some is stored in the muscle. The remaining vitamin E is found in
cell membranes in tissue.
Vitamin E is an antioxidant and one of the body's primary defenders against oxidative damage caused
by free radicals. Its activity is enhanced by other antioxidants such as vitamin C and the mineral
selenium. Vitamin E interrupts free-radical chain reactions by getting oxidized, thus protecting cell
membranes from free-radical attack. Scientists have implicated oxidative stress in the development of
cancer, arthritis, cataracts, heart disease, and in the process of aging itself. However, it is not yet known
whether supplementation with megadoses of vitamin E offers protection against heart disease and cancer
beyond that provided by positive dietary and lifestyle changes.
Deficiency.
Due to the widespread use of vegetable oils, primary vitamin-E deficiency is rare. Most deficiencies occur
in people with fat malabsorption syndrome. Smokers and adults on very low-fat diets are at increased
risk of developing vitamin-E deficiency. Preterm infants are particularly susceptible to hemolytic anemia
(anemia caused by the destruction of red blood cells) due to vitamin-E deficiency. These infants are born
with limited stores of vitamin E, which are exhausted by rapid growth, and they are inefficient in
absorbing vitamin E from the intestinal tract. Without vitamin E to protect against oxidation, the
destruction of cell membranes causes red blood cells to burst. To prevent hemolytic anemia, special
formulas and supplements containing vitamin E are prescribed for preterm infants.
Toxicity.
Large doses of vitamin E can counter the actions of vitamin K and decrease the production of vitamin K–
dependent clotting factors, thus promoting serious hemorrhaging effects in adults. Individuals who are
vitamin-K deficient or who are taking anticoagulant medications such as warfarin or aspirin are
especially at risk from megadoses of vitamin E.
SEE ALSO VITAMINS, WATER-SOLUBLE.
Kiran B. Misra
Bibliography
Insel, Paul; Turner, Elaine R.; and Ross, Don (2002). Nutrition. Sudbury, MA: Jones and Bartlett.
Wardlaw, Gordon M.; Hampl, Jeffrey S.; and Disilvestro, Robert A. (2004). Perspectives in Nutrition, 6th
edition. New York: McGraw-Hill.
Whitney, Eleanor Noss, and Rolfes, Sharon Rady (2002). Understanding Nutrition, 9th edition. Belmont,
CA: Wadsworth/Thomson Learning.
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no. 9.315
Fat-Soluble Vitamins
by J. Anderson and L. Young1
Quick Facts...





Small amounts of vitamins A, D, E and K are needed to maintain good health.
Foods that contain these vitamins will not lose them when cooked.
The body does not need these every day and stores them in the liver when not used.
Most people do not need vitamin supplements.
Megadoses of vitamins A, D, E or K can be toxic and lead to health problems.
Vitamins are essential nutrients your body needs in small amounts for various roles in the human
body. Vitamins are divided into two groups: water-soluble (B-complex and C) and fat-soluble (A, D, E
and K). Unlike water-soluble vitamins that need regular replacement in the body, fat-soluble vitamins
are stored in the liver and fatty tissues, and are eliminated much more slowly than water-soluble
vitamins.
Because fat-soluble vitamins are stored for long periods, they generally pose a greater risk for toxicity
than water-soluble vitamins when consumed in excess. Eating a normal, well-balanced diet will not
lead to toxicity in otherwise healthy individuals. However, taking vitamin supplements that contain
mega doses of vitamins A, D, E and K may lead to toxicity. Remember, the body only needs small
amounts of any vitamin.
While diseases caused by a lack of fat-soluble vitamins are rare in the United States, symptoms of
mild deficiency can develop without adequate amounts of vitamins in the diet. Additionally, some
health problems may decrease the absorption of fat, and in turn, decrease the absorption of vitamins
A, D, E and K. Consult your doctor about this.
Table 1 lists sources of fat-soluble vitamins, their basic functions in the body, major deficiency
symptoms caused by a lack of these vitamins, and symptoms of over-consumption.
Vitamin A
Vitamin A, also called retinol, has many functions in the body. In addition to helping the eyes adjust
to light changes, vitamin A plays an important role in bone growth, tooth development, reproduction,
cell division and gene expression. Also, the skin, eyes and mucous membranes of the mouth, nose,
throat and lungs depend on vitamin A to remain moist.
The best way to ensure your body gets enough vitamin A is to eat a variety of foods. Vitamin A is
supplied primarily by certain foods of animal origin like dairy products, fish and liver. Some foods of
plant origin contain beta-carotene, an antioxidant that the body converts to vitamin A. Beta-carotene,
or provitamin A, comes from fruits and vegetables. Carrots, pumpkin, winter squash, dark green leafy
vegetables and apricots are rich sources of beta-carotene.
The recommendation for vitamin A intake is expressed as micrograms (mcg) of retinol activity
equivalents (RAE). Retinol activity equivalents account for the fact that the body converts only a
portion of beta-carotene to retinol. One RAE equals 1 mcg of retinol or 12 mcg of beta-carotene (see
Table 2).
True vitamin A deficiency in the United States is rare. Night blindness and very dry, rough skin may
indicate a lack of vitamin A. Other signs of possible vitamin A deficiency include decreased resistance
to infections, faulty tooth development, and slower bone growth.
In the United States, toxic or excess levels of vitamin A are of more concern than deficiencies. The
tolerable upper intake level for adults is 3,000 mcg RAE. It would be difficult to reach this level
consuming food alone. But some multivitamin supplements contain high doses of vitamin A. If you
take a multivitamin, check the label to be sure the majority of vitamin A provided is in the form of
beta-carotene, which appears to be safe. Symptoms of vitamin A toxicity include dry, itchy skin,
headache, nausea, and loss of appetite. Signs of severe overuse over a short period of time include
dizziness, blurred vision and slowed growth. Vitamin A toxicity also can cause severe birth defects
and may increase the risk for hip fractures.
Physicians sometimes recommend that young infants take vitamin supplements that contain vitamin
A. However, toddlers and children need protection from too much vitamin A due to their smaller
body size. Typical foods eaten in large amounts by toddlers and children usually contain sufficient
amounts of vitamin A. Provide a variety of foods for your children, and if in doubt, check with a
pediatrician or Registered Dietitian.
Table 1: Vitamin facts.
Vitamin
Source
Physiological Functions Deficiency
Overconsumption
A
(retinol)
(provitamin
A, such as
beta
carotene)
Vitamin A: liver,
vitamin
A
fortified milk and
dairy products,
butter,
whole
milk, cheese, egg
yolk.
Provitamin
A:
carrots,
leafy
Helps to form skin and
mucous membranes and
keep them healthy, thus
increasing resistance to
infections; essential for
night vision; promotes
bones
and
tooth
development.
Beta
carotene
is
an
Mild:
nausea,
irritability,
blurred
vision.
Severe:
growth
retardation,
enlargement of liver
and spleen, loss of hair,
bone pain, increased
pressure in skull, skin
Mild:
night
blindness,
diarrhea,
intestinal
infections,
impaired vision.
Severe:
inflammation of
eyes,
green vegetables, antioxidant and may
sweet potatoes, protect against cancer.
pumpkins,
winter
squash,
apricots,
cantaloupe.
keratinization of changes.
skin and eyes.
Blindness
in
children.
D
Vitamin
Dfortified
dairy
products,
fortified
margarine, fish
oils, egg yolk.
Synthesized by
sunlight action
on skin.
Promotes hardening of
bones
and
teeth,
increases the absorption
of calcium.
Severe: rickets in Mild: nausea, weight
children;
loss,
irritability.
osteomalacia in Severe: mental and
adults.
physical
growth
retardation,
kidney
damage, movement of
calcium from bones
into soft tissues.
E
Vegetable
oil,
margarine,
butter,
shortening, green
and
leafy
vegetables,
wheat
germ,
whole
grain
products, nuts,
egg yolk, liver.
Protects vitamins A and Almost
C and fatty acids; impossible
to
prevents damage to cell produce without
membranes.
starvation;
Antioxidant.
possible anemia
in low birthweight infants.
K
Dark green leafy Helps blood to clot.
vegetables, liver;
also made by
bacteria in the
intestine.
Excessive
bleeding.
Nontoxic under normal
conditions.
Severe:
nausea,
digestive
tract
disorders.
None reported.
Vitamin D
Vitamin D plays a critical role in the body’s use of calcium and phosphorous. It increases the amount
of calcium absorbed from the small intestine and helps form and maintain bones. Children especially
need adequate amounts of vitamin D to develop strong bones and healthy teeth.
The primary food sources of vitamin D are milk and other dairy products fortified with vitamin D.
Vitamin D is also found in oily fish (e.g., herring, salmon and sardines) as well as in cod liver oil. In
addition to the vitamin D provided by food, we obtain vitamin D through our skin which makes
vitamin D in response to sunlight.
An Adequate Intake (AI) for has been established for vitamin D (see Table 2). The AIs for vitamin D
appear as micrograms (mcg) of cholecalciferol. Ten mcg of cholecalciferol equals 400 International
Units (IU).
Symptoms of vitamin D deficiency in growing children include rickets (long, soft bowed legs) and
flattening of the back of the skull. Vitamin D deficiency in adults is called osteomalacia, which results
in muscular weakness and weak bones. These conditions are rare in the United States.
The tolerable upper intake level for vitamin D is set at 50 mcg for people 1 year of age and older (see
Table 3). High doses of vitamin D supplements coupled with large amounts of fortified foods may
cause accumulations in the liver and produce signs of poisoning. Signs of vitamin D toxicity include
excess calcium in the blood, slowed mental and physical growth, decreased appetite, nausea and
vomiting.
It is important that infants and young children do not consume excess amounts of vitamin D
regularly. Children exposed to the sun for 5 to 10 minutes daily will produce enough vitamin D.
However, if children live in inner cities, wear clothes that cover most of their skin or live in northern
climates where little sun is seen in the winter, then vitamin D deficiency may occur. Rather than give
children a supplement, add fortified foods to their diet, such as vitamin D fortified milk and other
dairy products.
Table 2: Dietary Reference Intakes (DRI) for fat soluble vitamins.
Life
Vitamin Vitamin Vitamin Vitamin Vitamin
E Vitamin E (IU)
Stage A
A (IU) D
D (IU) (mg a-TE3)
Group (mcg1)
(mcg2)
Infants
0.0-0.5 400*
1333
5*
200
4*
6
0.5-1.0 500*
1666
5*
200
5*
7.5
Children 1-3
300
1000
5*
200
6
9
4-8
400
1333
5*
200
7
10.5
9-13
600
2000
5*
200
11
16.5
14-18
900
3000
5*
200
15
22.5
19-30
900
3000
5*
200
15
22.5
31-50
900
3000
5*
200
15
22.5
51-70
900
3000
10*
400
15
22.5
71+
900
3000
15*
600
15
22.5
Females 9-13
600
2000
5*
200
11
16.5
14-18
700
2333
5*
200
15
22.5
19-30
700
2333
5*
200
15
22.5
31-50
700
2333
5*
200
15
22.5
51-70
700
2333
10*
400
15
22.5
71+
700
2333
15*
600
15
22.5
Pregnant <18
750
2500
5*
200
15
22.5
19-30
770
2566
5*
200
15
22.5
31-50
770
5*
200
15
22.5
Males
Lactating <18
1,300
4000
5*
200
19
28.8
19-30
1,300
4333
5*
200
19
28.8
31-50
1,300
4333
5*
200
19
28.8
*Indicates an Adequate Intake (AI). All other values are Recommended Dietary Allowance
(RDA).
1As retinol activity equivalents (RAEs). 1 RAE = 1mcg retinol or 12 mcg beta-carotene.
2
As cholecalciferol. 10 mcg cholecalciferol = 400 IU of vitamin D.
3 As alpha-tocopherol equivalents. 1 mg of alpha-tocopherol = 1.5 IU of vitamin E.
Vitamin E
Vitamin E acts as an antioxidant, protecting vitamins A and C, red blood cells and essential fatty acids
from destruction. Research from a decade ago suggested that taking antioxidant supplements, vitamin
E in particular, might help prevent heart disease and cancer. However, newer findings indicate that
people who take antioxidant supplements are not better protected against heart disease and cancer
than non-supplement users. On the other hand, there are many studies that show a link between
regularly eating antioxidant-rich fruits and vegetables and a lower risk for heart disease, cancer and
several other diseases.
The RDA for vitamin E is based on the most active and usable form called alpha-tocopherol (see Table
2). One milligram of alpha-tocopherol equals to 1.5 International Units (IU).About 60 percent of
vitamin E in the diet comes from vegetable oil or products made with vegetable oils. Therefore, good
food sources of vitamin E include vegetable oils and margarines. Vitamin E is also found in fruits and
vegetables,
grains,
nuts,
seeds
and
fortified
cereals.
Vitamin E deficiency is rare. Cases of vitamin E deficiency only occur in premature infants and people
unable to absorb fats.
The tolerable upper intake levels for vitamin E are shown in Table 3. Large doses of vitamin E pose a
hazard to people who take blood-thinning medications. People taking statin drugs are also not
advised to take supplemental vitamin E because it may interfere with how the medication works.
Vitamin K
Naturally produced by the bacteria in the intestines, vitamin K plays an essential role in normal blood
clotting and helps promote bone health.
Good food sources of vitamin K are green vegetables such as turnip greens, spinach, cauliflower,
cabbage and broccoli, and certain vegetables oils including soybean oil, cottonseed oil, canola oil and
olive oil. Animal foods, in general, contain limited amounts of vitamin K.
To help ensure people receive sufficient amounts of vitamin K, an Adequate Intake (AI) has been
established for each age group (see Table 2).
Without sufficient amounts of vitamin K, hemorrhaging can occur. Deficiencies may appear in infants,
or in people who take anticoagulants or antibiotic drugs. Newborn babies lack the intestinal bacteria
to produce vitamin K and need a supplement for the first week. People on anticoagulant drugs (blood
thinners) may become deficient in vitamin K, but should not change their vitamin K intake without
consulting a physician because the effectiveness of the drug may be affected. People taking antibiotics
may lack vitamin K temporarily because intestinal bacteria are sometimes killed as a result of longterm use of antibiotics. Also, people with chronic diarrhea may have problems absorbing sufficient
amounts of vitamin K through the intestine and should consult their physician to determine if
supplementation is necessary.
Although a tolerable upper intake level has not been established for vitamin K, excessive amounts can
cause the breakdown of red blood cells and liver damage. Large doses are not advised.
Table 3. Tolerable upper intake levels (UL)*.
Life
Stage Vitamin A Vitamin
Group
(mcg)
(mcg)
Infants
Children
Males/Females
Pregnant
Lactating
D Vitamin E (mg
a-TE)
0.0-0.5
600
25
ND1
0.5-1.0
600
25
ND
1-3
600
50
200
4-8
900
50
300
9-13
1,700
50
600
14-18
2,800
50
800
19-70
3,000
50
1,000
>71
3,000
50
1,000
& <18
2,800
50
800
3,000
50
1,000
19-50
*A
UL
for
vitamin
K
was
1ND = not determinable due to insufficient data.
not
established.
Standards for Measuring Intake
Vitamin requirements are expressed in small units. Most are given in milligrams (mg) or micrograms
(mcg). When comparing vitamin amounts on labels, note whether values are in micrograms (mcg),
milligrams (mg) or International Units (IU). Make sure you compare the same units.
Dietary Reference Intakes (DRI) are dietary standards for desirable and/or safe vitamin intake levels
published by the Food and Nutrition Board of the National Academy of Sciences National Research
Council. DRIs include three sets of values: recommended dietary allowances (referred to as RDAs)
which are intended to meet the nutrient needs of healthy individuals; tolerable upper intake levels
(UL) which are designed to help people avoid harmful effects caused by consuming too much of a
nutrient; and adequate intakes (AI), which are established when there is not enough scientific
evidence to set an RDA and are based on diets known to be nutritionally adequate for U.S. and
Canadian populations. Table 2 lists the recommended amounts of fat-soluble vitamins that
individuals in the United States need daily for good health. Table 3 provides the tolerable upper
intake levels.
References






Complete Book of vitamins and Minerals (2000). Publications International, Ltd.
Facts About Dietary Supplements (2001). NIH Clinical Center. Available on
www.cc.nih.gov/ccc/supplements/intro.html
Insel, P. et al (2001). Nutrition. Sudbury, MA: Jones and Bartlett publishers.
Dietary Reference intakes for Calcium, Phosphorus, Magnesium, Vitamin D and Fluoride.
Washington, DC: National Academy Press, 1997.
Dietary Reference Intakes for Vitamin C, Vitamin E, Selenium, and Carotenoids. Washington, DC:
National Academy Press, 2000.
Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron,
Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc. Washington, DC: National
Academy Press, 2001
J. Anderson, Colorado State University Extension food and nutrition specialist and professor,
food science and human nutrition; and L. Young, M.S., former graduate student. 7/96. Revised
5/06.
1
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